Manifestations Of Ischemic Heart Disease Research Articles

Agenesia del tronco coronario izquierdo. Descripción de un caso y revisión de la bibliografía

Clinical and angiographic features are described in a fifty-five years old man, with long-standing clinical manifestations of ischemic heart disease. In addition to severe coronary atherosclerosis, congenital atresia of the left main coronary was present. A description of the coronary anomaly found and a discussion of its meaning and significance are presented.

ACE gene polymorphism: ischemic heart disease and longevity in 10,150 individuals. A case-referent and retrospective cohort study based on the Copenhagen City Heart Study.

Homozygosity for the deletion allele (D) of the angiotensin-converting enzyme (ACE) gene insertion-deletion polymorphism has been suggested to be a potent risk factor for myocardial infarction. With one exception, the samples studied so far have been small and/or ethnically heterogeneous, and most investigators have studied men only. We investigated the association between ACE genotype and myocardial infarction as well as other manifestations of ischemic heart disease for both women and men in a case-referent study (n = 10,150) as well as in a retrospective cohort study (n = 7263). The cohort was from the ethnically homogeneous Danish population. Case subjects were from the same geographic area and had ischemic heart disease. Irrespective of the assumed degree of relative penetrance of the D allele, the odds ratios were not significantly different from 1.0 (P > .05) for ischemic heart disease, severe stenosis on coronary angiography, or myocardial infarction. There was also no association between ACE genotype and phenotypic variation in recognized risk factors for ischemic heart disease. Finally, the relative frequency of the D allele did not change as a function of age in subjects aged from 20 to > or = 80 years. In two large studies, a case-referent study and a retrospective cohort study in an ethnically homogeneous white population, there was no evidence for a statistically significant difference in the development of myocardial infarction or any other manifestations of ischemic heart disease between genotype classes of the ACE gene polymorphism in either women or men.

Relationship of peak expiratory flow rate with mortality and ischaemic heart disease in elderly Australians.

To evaluate the relationships of mortality and ischaemic heart disease (IHD) with peak expiratory flow rate (PEF) in the elderly. Prospective study with median follow-up of 83 months. Dubbo, a New South Wales country town (population, 30500). Non-institutionalised residents born before 1930 (i.e., aged 60 years and over at study entry). Participation rate was 73% (1235 men and 1570 women). Baseline demographic, psychosocial and standard cardiovascular risk factors, including PEF; all-causes mortality, IHD mortality and IHD events (hospitalisations with any manifestation of IHD) by tertile of PEF. More subjects with PEF in the lowest tertile (I) had a past history of respiratory disease, were current cigarette smokers and were taking antihypertensive drugs. During follow-up, 321 men (26%) and 252 women (16%) died. All-causes mortality was three (men) to four (women) times higher for those in PEF tertile I than for those in tertile III. IHD mortality and IHD events showed similar trends. In a proportional hazards model adjusted for age, height, smoking status and other risk factors or confounders, the hazard ratios (95% confidence interval) for men in PEF tertile I versus tertile III were: all-causes mortality, 1.62 (1.14-2.30); IHD mortality, 1.75 (0.96-3.20); and IHD events, 1.12 (0.82-1.53). For women, respective hazard ratios were 1.92 (1.23-3.00), 2.58 (1.24-5.39), and 1.16 (0.83-1.63). We confirm an independent, inverse relationship between PEF and all-causes and IHD mortality. The data suggest a potential benefit for coronary risk factor management in subjects with existing airways disease and further support the case for antismoking programs.

Inflammation in ischaemic heart disease

Recent reports have suggested a link between blood concentrations of C reactive protein and the risk of cardiovascular disease. The ECAT study (European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study) followed 3000 people with chronic stable ischaemic heart disease for three years and found a significant correlation between concentrations of C reactive protein within the normal range and long term cardiovascular risk.1 Raised concentrations have also been shown to be strong prognostic indicators in patients with unstable angina,2 and in this week's BMJ Mendall et al report an association between C reactive protein concentrations and indirect evidence of ischaemic heart disease (p1061).3 What are the pathogenetic implications of this novel marker of acute and chronic manifestations of ischaemic heart disease and its relevance in clinical practice? Mendall et al studied 303 men aged 50-69 years selected from general practice registers3 and found that the prevalence of indirect evidence of ischaemic heart disease and a history of claudication (together with age, smoking, chronic bronchitis, and most traditional cardiovascular risk factors) increased progressively as blood concentrations of C reactive protein rose. This correlation between C reactive protein and traditional risk factors for ischaemic heart disease may influence prognosis in the long term by favouring the development of atherosclerosis, but the prognostic value of C reactive protein might also result from an increased incidence and worse outcome of …

A Prospective Evaluation of an Angiotensin-Converting–Enzyme Gene Polymorphism and the Risk of Ischemic Heart Disease

In a previous study, men with a history of myocardial infarction were found to have an increased prevalence of homozygosity for the deletional allele (D) of the angiotensin-converting-enzyme (ACE) gene. The D allele is associated with higher levels of ACE, which may predispose a person to ischemic heart disease. We investigated the association between the ACE genotype and the incidence of myocardial infarction, as well as other manifestations of ischemic heart disease, in a large, prospective cohort of U.S. male physicians. In the Physicians' Health Study, ischemic heart disease as defined by angina, coronary revascularization, or myocardial infarction developed in 1250 men by 1992. They were matched with 2340 controls according to age and smoking history. Zygosity for the deletion-insertion (D-I) polymorphism of the ACE gene was determined by an assay based on the polymerase chain reaction. Data were analyzed for both matched pairs and unmatched samples, with adjustment for the effects of known or suspected risk factors by conditional and nonconditional logistic regression, respectively. The ACE genotype was not associated with the occurrence of either ischemic heart disease or myocardial infarction. The adjusted relative risk associated with the D allele was 1.07 (95 percent confidence interval, 0.96 to 1.19; P = 0.24) for ischemic heart disease and 1.05 (95 percent confidence interval, 0.89 to 1.25; P = 0.56) for myocardial infarction, if an additive mode of inheritance is assumed. Additional analyses assuming dominant and recessive effects of the D allele also failed to show any association, as did the examination of low-risk subgroups. In a large, prospectively followed population of U.S. male physicians, the presence of the D allele of the ACE gene conferred no appreciable increase in the risk of ischemic heart disease or myocardial infarction.

Fibrinogen in ischaemic heart disease.

Fibrinogen contributes to both pathological and clinical manifestations of ischaemic heart disease (IHD). Several cross-sectional angiographic studies have shown correlations between the fibrinogen level and the extent of coronary artery disease. The largest of these studies suggests that this relationship is due mainly to luminal occlusion, strengthening the evidence that high fibrinogen levels are thrombogenic. The growing number of prospective studies that have included fibrinogen measurements consistently show a direct, independent and statistically significant association between fibrinogen level and the subsequent incidence of IHD, this association being about as strong as the relation between cholesterol and IHD, for example. The fibrinogen level is also associated with the recurrence of IHD in those who have survived a myocardial infarction and with the onset and recurrence or progression of cerebrovascular disease and lower extremity arterial disease. Besides a contribution to coronary artery changes, high fibrinogen levels predispose to IHD through influences on blood and plasma viscosity, platelet aggregability and the amount of fibrin produced when coagulation is initiated. Progress towards the standardization of methods for measuring fibrinogen increasingly justifies its inclusion in the IHD risk profile. Establishing the value of agents that lower fibrinogen levels is now a high research priority, mainly for clinical reasons but also as part of the evidence for clarifying the nature of the association of raised levels with arterial disease.

Acute ischemic syndromes

The diagnosis and treatment of patients with acute manifestations of ischemic heart disease are major public health issues. This article reviews the current state of knowledge about the problem of acute ischemic syndromes, the events leading to clinical manifestations, the key elements of the diagnosis, the therapies that can affect outcome, and the organization of systems to deal with this problem in a cost-effective manner.

Five-year follow-up of microsurgical multiple internal thoracic artery grafts

In a consecutive series of 143 patients requiring multiple coronary artery bypass grafts, 317 of 441 anastomoses (72%) were constructed from internal thoracic arteries. Of these 143 patients, 103 had bilateral, 51 sequential, and 49 free internal thoracic artery grafts. When compared with an earlier series of 494 patients who underwent only one internal thoracic artery anastomosis, the surgical morbidity and mortality were not increased, but, during 5 years of follow-up, the incidences of postoperative angina and myocardial infarction were found to decrease significantly—32.5% versus 10.5% ( p < 0.001) and 5.7% versus 1.4% ( P < 0.03), respectively. We conclude that, for patients with multivessel disease, multiple internal thoracic artery grafts confer better protection from the clinical manifestations of ischemic heart disease than does one internal thoracic artery graft. The use of high magnification (8 to 12X, surgical microscope) was essential to the success of this method.

Increased expression of neutrophil and monocyte adhesion molecules in unstable coronary artery disease.

A rapid increase in leukocyte adhesion to endothelial cells is one of the first events in the acute inflammatory response and in the pathogenesis of vascular diseases. A subgroup of cell surface glycoproteins (the CD11/CD18 complex) play a major role in the leukocyte adhesion process; in particular, the CD11b/CD18 receptor can be upregulated severalfold in response to chemotactic factors. The purpose of this study was to assess whether upmodulation of granulocyte and monocyte CD11b/CD18 receptors takes place during the passage of blood through the coronary tree of patients with clinical manifestations of ischemic heart disease. Thirty-nine patients who underwent diagnostic coronary arteriography were studied. Group 1 (15 patients) had a clinical diagnosis of unstable angina, group 2 (14 patients) had stable exertional angina, and group 3 (10 patients) had atypical chest pain. Simultaneous sampling from the coronary sinus and aorta was obtained before coronary arteriography. Cell surface receptors were detected by direct immunofluorescence evaluated by flow cytofluorimetry using monoclonal antibodies tagged with fluorescent markers. Leukocytes were stained in unseparated blood to avoid in vitro manipulation that could activate phagocytes. Group 1 and 2 patients had significant coronary artery disease (> 50% coronary narrowing in at least one major coronary vessel), whereas group 3 patients had normal coronary arteries. In group 1, granulocytes and monocytes showed a significantly higher expression of the CD11b/CD18 adhesion receptor in the coronary sinus than in the aorta (both P < .01), whereas no difference in CD11b/CD18 expression was seen in groups 2 and 3. Patients with unstable angina have an increased expression of granulocyte and monocyte CD11b/CD18 adhesion receptors, indicating that an inflammatory reaction takes place within their coronary tree. Activation of these leukocytes may induce coronary vasoconstriction, favor thrombotic processes, and further activate platelets, thus having potential implications on the pathogenesis of unstable coronary artery disease.

Comparison of coronary angiographic findings in acute and chronic first presentation of ischemic heart disease.

It is generally assumed that the clinical manifestations of ischemic heart disease occur randomly on the same underlying pathological process. Therefore, coronary angiographic findings should be similar whether the first presentation of ischemic heart disease is acute myocardial infarction or uncomplicated chronic stable angina. We studied 102 patients (men < or = 60 years old, women < or = 65 years old) presenting with either acute myocardial infarction as first manifestation of coronary artery disease with a concomitant coronary angiogram (55 patients; mean age, 50.2 years) or stable angina for at least 2 years with no history, ECG, or left ventriculographic evidence of any acute event and with an angiogram performed at least 2 years after initial symptoms (47 patients; mean age at symptom onset, 51.7 years). These angiograms were evaluated blindly for severity (number of vessels diseased, stenoses > or = 50%, occlusions), extent of disease (with an index derived by assigning a score of 0-3 per segment, depending on the proportion of lumen length irregularity and dividing the sum by the number of visualized segments), and pattern (discrete: three or fewer loci of disease never involving more than 50% of the length of any segment or diffuse: anything exceeding this). Patients with unheralded myocardial infarction had fewer vessels diseased, fewer stenoses and occlusion, and a lower extent index than those with uncomplicated stable angina (mean +/- SD of 1.3 +/- 0.8 versus 2.1 +/- 0.8, p < 0.001; 2.1 +/- 1.8 versus 3.9 +/- 1.8, p < 0.001; 0.6 +/- 0.6 versus 1.0 +/- 0.9, p < 0.02; and 0.6 +/- 0.5 versus 1.2 +/- 0.5, p < 0.001, respectively). A discrete pattern was present in 54.5% of patients with unheralded infarction and in only 8.5% of those with uncomplicated angina (p < 0.001). These very different angiographic findings suggest that unheralded acute myocardial infarction and uncomplicated chronic stable angina do not occur randomly on a common atherosclerotic background but rather that additional factors, such as a varying propensity to thrombosis, may predispose to one or the other of these two clinical syndromes.

Left ventricular assistance without thoracotomy: Mediastinal and transseptal approaches to the left heart

Two methods to cannulate the left atrium for initiating mechanical left ventricular circulatory assistance using a centrifugal pump were investigated in 25 sheep. A modified Dennis transatrial septal approach produced flow rates of 88.6 ± 14 mL · kg −1 · min −1 through 21F catheters inserted during fluoroscopy through the jugular vein. In 8 animals the septal perforation was plugged after decannulation with a modified Rashkind umbrella plug. Fibroendothelial tissue covered the plug by 4 weeks. In 7 other animals, the septal defect was not plugged. The septal defect reached pinpoint size by 2 weeks and was completely closed by 4 weeks. In 10 sheep, the left atrium was cannulated from the neck through the mediastinum. Left ventricular assistance flow averaged 71.6 ± 14 mL · kg −1 · min −1. Mean blood loss during 1 hour of left ventricular assistance was 47 mL. In 8 animals, the atrial perforation was plugged with a mean blood loss of 253 ± 194 mL. In 2 animals, the perforation was intentionally not plugged; mean blood loss was 700 mL. All animals survived. The modified Dennis transatrial method is recommended as a safe, expeditious, cost-effective method to implement left ventricular assistance without thoracotomy. The mediastinal approach, which is technically possible in humans, is more difficult but feasible. Left ventricular assistance has been proven to be the most effective way to rest the failing, ejecting left ventricle. Implementation without thoracotomy potentially expands applications of left ventricular assistance for temporary support of patients with severe manifestations of ischemic heart disease.

Granulocyte function in coronary artery disease

Granulocytes defend the body against invading microbes by producing a complex armamentarium of toxic substances, such as proteolytic enzymes, oxygen radicals and arachidonic acid metabolites. Under certain circumstances, however, such compounds may be released in the absence of phagocytosabte particles, resulting in injury to normal cell and connective tissue degradation. Recent experimental studies have emphasized the potential role of granulocytes in the pathogenesis of myocardial ischemia. Clinical investigations have also shown alterations in neutrophil function in stable and unstable clinical manifestations of ischemic heart disease. “Priming” of granulocytes in stable forms of coronary disease may predispose to the subsequent development of acute coronary events, whereas activation of neutrophils may lead to alterations in vascular permeability and coronary flow regulation, leading to further myocardial and endothelial injury in acute myocardial infarction, unstable angina and coronary angioplasty.

Factors influencing the formation of new human coronary lesions: age, blood pressure, and blood cholesterol.

The Cholesterol Lowering Atherosclerosis Study, a controlled angiographic trial, has reported that new native coronary artery lesions are significantly reduced by aggressive blood lipid lowering therapy with colestipol plus niacin. To study factors relevant to primary atherosclerosis prevention, we have conducted an epidemiologic analysis of new native coronary lesion formation in placebo-treated patients. Univariate and multivariate logistic regression procedures were used to examine age at entry into the study, number of years since bypass, body weight, diastolic and systolic blood pressure, plasma total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, non-HDL-cholesterol, and apolipoproteins A-I,B, and C-III. Significant univariate protective factors were older age (P less than .006), reduction of total plasma cholesterol (P less than .040), and systolic (P less than .024) and diastolic (P less than .022) blood pressure. Significant multivariate protective factors were older age (P less than .005) and reduction in systotic blood pressure (P less than .021). Blood pressure effects were not associated with use of specific antihypertensive agents. These data provide additional support for the control of hypertension and reduction of blood cholesterol level for primary and secondary ischemic heart disease prevention. They also indicate the existence of a population at high risk for early coronary lesion formation and the need for improved means to identify such individuals prior to the onset of clinical manifestations of ischemic heart disease.

Ten-year follow-up of quality of life in patients randomized to receive medical therapy or coronary artery bypass graft surgery. The Coronary Artery Surgery Study (CASS)

Quality of life indexes were assessed in 780 patients 10 years after randomization to medical therapy (n = 390) or coronary artery bypass graft surgery (n = 390) in the Coronary Artery Surgery Study. At 10 years, mortality was 21.8% in the medical group and 19.2% in the surgical group (p = NS), and 144 (37%) of the medical group had undergone surgery because of increasing chest pain. At study entry, 22% of medical and surgical patients were angina free; at 1 and 5 years after entry, the frequency of asymptomatic patients was 66% and 63% in the surgical group and 30% and 38% in the medical group. However, by 10 years after entry, the proportion of patients free of angina had fallen to 47% in the surgical group and to 42% in the medical group. Activity limitation and use of beta-blockers and long-acting nitrates were less in the surgical than the medical group at 1 and 5 years after entry but little different from the medical group at 10 years after entry. Throughout follow-up, recreational status, employment status, frequency of heart failure, use of other medications, and hospitalization frequency were similar between the two groups. Thus, indexes of quality of life such as angina relief, increased activity, and reduction in use of antianginal medications initially appear superior in patients with stable manifestations of ischemic heart disease assigned to surgery, but by 10 years after entry, these advantages are much less apparent. Although the observed similarities of the medically and surgically assigned groups at 10 years reflect return of symptoms in the surgical group to some extent, a more important explanation is the performance of late surgery in a large proportion of the medically assigned patients, rendering them asymptomatic.

Neurohumoral activation during acute myocardial ischaemia. Effects of ACE inhibition

ACE inhibition may be useful in several manifestations of ischaemic heart disease, such as heart failure due to ischaemic cardiomyopathy. Recent evidence suggests that these effects may also be present in normotensive patients with ischaemic heart disease without heart failure. Theoretically, converting-enzyme inhibition, through coronary and systemic vasodilating effects and negative inotropic properties, should have a favourable effect on the myocardial oxygen supply/demand ratio and, hence, affect the incidence and severity of myocardial ischaemia. It is doubtful, however, whether these cardiac and extracardiac properties of ACE inhibitors really underlie its potential antiischaemic effects, at least in the average patient with ischaemic heart disease without concomitant heart failure and hypertension. Recent animal and human studies indicate that converting-enzyme inhibitors may modulate myocardial ischaemia by reducing ischaemia-induced circulating neurohumoral activation. It has been shown that, depending on the severity of ischaemia, the circulating renin-angiotensin system may become activated together with an increase in circulating catecholamine levels. ACE inhibition suppresses this neuroendocrine stimulation during ischaemia and modulates subsequent systemic and, presumably, also coronary vasoconstriction. In addition to these effects on circulating neurohormones, ACE inhibition could affect myocardial ischaemia through a number of local actions, e.g. modulation of tissue (cardiac) angiotensin II formation and bradykinin breakdown, stimulation of prostaglandin synthesis and, in the use of sulphydryl compounds, by affecting EDRF formation. Whether ACE inhibitors have clear antiischaemic effects in all clinical conditions is uncertain. Their efficacy to limit exercise-induced ischaemia has been questioned. In contrast, pacing-induced ischaemia in patients at rest is clearly prevented by ACE inhibition. This differential effect may be related to a more pronounced difference in circulating neurohormones during exercise per se. It also suggests that ACE inhibitors may be particularly useful as (additional) antiischaemic therapy in patients with angina at rest, e.g. unstable angina and the acute phase of myocardial infarction.

Early evolution of symptoms and long-term prognosis in variant angina: Importance of the functional component of coronary arterial disease

Purpose: Most investigations describing the long-term outcome of large groups of patients with variant angina pectoris have focused on such endpoints as myocardial infarction, coronary artery surgery, and death, and have asked how the risk of these events is related to the severity of existing organic coronary disease. It is also possible to ask what is the relative importance of organic and functional components in causation of symptoms and outcomes, as was done in this study. Patients and methods: The early and long-term clinical course was observed in a group of 80 patients with variant angina and a low prevalence of severe organic coronary disease (diameter stenosis greater than 70 percent of one vessel in 28.3 percent, of two or more vessels in 2.7 percent). Patients were seen at the UCLA Medical Center between July 1963 and June 1985. Results: The following observations were made: Compared with those experiencing a first episode of angina at rest, subjects whose first episode of vasospastic angina occurred during strenuous effort were more likely subsequently to have a positive exercise test result and a more stable but long-term anginal course. A good initial response to vasodilator therapy indicated a likelihood of being alive and symptom-free without an intervening myocardial infarction by five years after diagnosis, which was twice the rate as if initial response to such treatment was poor. The presence or absence of severe coronary artery obstruction as detected by angiography could not be predicted from the nature or severity of angina, the historical presence of effort angina, or the occurrence of a positive result on an exercise test. The existence of severe coronary stenosis in at least one vessel was not associated with an increased incidence of myocardial infarction, cardiac arrest, or death in the first nine years after diagnosis. Conclusion: These findings are consistent with the hypothesis that manifestations of ischemic heart disease in these patients were more directly caused by coronary vasospasm than by the degree of organic coronary obstruction seen by coronary arteriography. In addition, the presence of severe organic stenosis in one coronary artery did not appear to be associated with measurably increased adverse effects on clinical course or survival over the first nine years after diagnosis.

Hypocholesterolemic activity of racemic dichlorophenoxypropionic acid or its enantiomers in rats.

Abundant circumstantial evidence has shown that chronic hyperlipidemia is one of the major clinical manifestations of ischemic heart disease (IHD) and many drugs have been developed which reduce serum lipids. Clofibrate has been one of the most effective drugs used for lowering serum cholesterol and reducing the morbidity of patients suffering from IHD. However, prolonged treatment with clofibrate has been reported to cause higher incidences of gastrointestinal disorders and to induce cholesterol oversaturation of bile. These deleterious side effects have resulted in a restriction of the use of clofibrate and new drugs exerting selective and non toxic hypolipidemic actions have been intensively researched. (Dichloro-2,4 phenoxy)-2 propionic acid, structurally-related to fibrates with an asymmetric carbon is well know for its herbicide effectiveness. However, nobody has investigated its possible effect on cholesterol /sup 14/C-acetate metabolism. The purpose of this study is to explore the effects of this compound on cholesterol metabolism in the rat and to compare them with those of clofibrate. It is the first time that a low concentration (0.04 mmole) of this well-known pesticide has been shown to lower plasma cholesterol when added to the diet.

Heart rate, employment status, and prevalent ischaemic heart disease confound relation between cereal fibre intake and blood pressure.

Cross sectional data from a survey of 2512 men aged 45-49 years were used to examine the confounding effects of heart rate, employment, and ischaemic heart disease (IHD) on the relation between cereal fibre intake and blood pressure. Daily cereal fibre intake (g/day) was associated with systolic pressure (r = -0.053, p less than 0.01), diastolic pressure (r = -0.057, p less than 0.01), and heart rate (r = -0.071, p less than 0.01). The associations were strengthened in employed men and inapparent in unemployed men. Unemployed men had more IHD than employed men. Persons with any manifestation of IHD had significantly higher blood pressure and heart rates but ate less cereal fibre (7.0 v 7.9 g/day, p less than 0.001) than those without IHD, regardless of employment status. In employed men, after adjustment for age, body mass index, prevalent IHD, and heart rate, systolic pressure changed -0.186 mmHg (95% CI = -0.362, -0.009) and diastolic pressure changed -0.111 mmHg (95% CI = 0.228, 0.005) for each gram of cereal fibre eaten daily. The association between cereal fibre and blood pressure was inapparent in unemployed men. Heart rate, employment, and prevalent IHD confound the association between cereal fibre intake and blood pressure. Future work concerning this relationship will have to account for the effects of these variables.

Abnormal thallium kinetics in postoperative coarctation of the aorta: Evidence for diffuse hypertension-induced vascular pathology

After operative correction of congenital coarctation of the aorta, patients continue to have excess cardiovascular mortality, including manifestations of ischemic heart disease. Previous morphologic studies support the concept of direct hypertensive vascular injury in these patients. To determine whether abnormalities of myocardial perfusion were present in an asymptomatic group of patients with coarctation repair, 18 men and 9 women with a mean age of 26 years (range 19 to 41) were studied between 2 and 25 years after operative correction. Stress electrocardiography and quantitative thallium imaging by a circumferential profile technique were used. These patients were compared with a normal group, statistically defined as having a less than 1% prevalence of significant obstructive coronary artery disease. The postoperative coarctation group demonstrated a reduction in global thallium redistribution in each view analyzed. As compared with findings in the control subjects, thallium washout in the anterior view (41.9 versus 48.6%, p = 0.02) and left anterior oblique projection (40.5 versus 48.2%, p = 0.007) was significantly diminished. Although the postoperative coarctation group had a lower thallium redistribution rate in the lateral view (41.4 versus 46.3%, p = 0.09) this difference did not reach statistical significance because of the intrinsic variability of this projection. Plots of the median percent thallium washout revealed independence from circumferential profile angle, indicating global abnormalities in perfusion. No correlation between clinical variables and thallium kinetics could be established, suggesting marked individual variability in the development of this vascular lesion. The observation of abnormal thallium kinetics in patients with coarctation repair may have consequences for long-term follow-up and therapy.

Psychosocial factors and risk of ischaemic heart disease and death in women: A twelve-year follow-up of participants in the population study of women in Gothenburg, Sweden

A community sample of 795 women of the ages 38, 46, 50 and 54 yr was subjected to comprehensive medical and psychiatric examinations and was followed up for 12 yr. The 12-yr incidence of angina pectoris was 3.2% and of electrocardiographic changes indicating ischaemic heart disease 5.8%. The corresponding incidence of myocardial infarction was 1.4% and death rate 4.2%. High initial ratings of passive dependency, neuroticism, experience of strain, grade of mental disorder and severity of major or minor depression were predictive of angina pectoris. A low rating of aggression was predictive of the development of electrocardiographic changes indicating ischaemic heart disease. Low ratings of guilt feelings and neurotic self-assertiveness were predictive of myocardial infarction. Death rate was not related to any of the psychosocial factors studied. These associations remained significant after adjustments for age, social class, marital status or confounding conventional risk factors for ischaemic heart disease. The results show that the different clinical manifestations of ischaemic heart disease are related to different sets of psychosocial predictors.